Modulation Of Reciprocal Inhibition Research Articles

Modulation of reciprocal inhibition at the wrist as a neurophysiological correlate of tremor suppression: a pilot healthy subject study.

It has been shown that Ia afferents inhibit muscle activity of the ipsilateral antagonist, a mechanism known as reciprocal inhibition. Stimulation of these afferents may be explored for the therapeutic reduction of pathological tremor (Essential Tremor or due Parkinson's Disease, for example). However, only a few studies have investigated reciprocal inhibition of wrist flexor / extensor motor control. The main goal of this study was to characterize reciprocal inhibition of wrist flexors / extensors by applying surface electrical stimulation to the radial and median nerves, respectively. Firstly, the direct (M) and monosynaptic (H) reflex responses to increasing median and radial nerve stimulation were recorded to characterize the recruitment curve of the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles, respectively. Based on the recruitment curve data, we then stimulated the median and radial nerves below (<; MT) and above (> MT) motor threshold (MT) during a submaximal isometric task to assess the amount of inhibition on ECR and FCR antagonist muscles, respectively. The stimulation of both nerves produced a long-duration inhibition of the antagonist motoneuron pool activity. On average, maximum peak of inhibition was 27 ± 6% for ECR and 32 ± 9% for FCR with stimulation <; MT; maximum peak of inhibition was 45 ± 7% for ECR and 44 ± 13% for FCR when using stimulation > MT. These results validate this neurophysiological technique that demonstrates a mechanism similar to classical reciprocal Ia inhibition reported for other limb joints and that can be used to benchmark strategies to suppress pathological tremor.

Hybrid Assistive Neuromuscular Dynamic Stimulation Therapy: A New Strategy for Improving Upper Extremity Function in Patients with Hemiparesis following Stroke.

Hybrid Assistive Neuromuscular Dynamic Stimulation (HANDS) therapy is one of the neurorehabilitation therapeutic approaches that facilitates the use of the paretic upper extremity (UE) in daily life by combining closed-loop electromyography- (EMG-) controlled neuromuscular electrical stimulation (NMES) with a wrist-hand splint. This closed-loop EMG-controlled NMES can change its stimulation intensity in direct proportion to the changes in voluntary generated EMG amplitudes recorded with surface electrodes placed on the target muscle. The stimulation was applied to the paretic finger extensors. Patients wore a wrist-hand splint and carried a portable stimulator in an arm holder for 8 hours during the daytime. The system was active for 8 hours, and patients were instructed to use their paretic hand as much as possible. HANDS therapy was conducted for 3 weeks. The patients were also instructed to practice bimanual activities in their daily lives. Paretic upper extremity motor function improved after 3 weeks of HANDS therapy. Functional improvement of upper extremity motor function and spasticity with HANDS therapy is based on the disinhibition of the affected hemisphere and modulation of reciprocal inhibition. HANDS therapy may offer a promising option for the management of the paretic UE in patients with stroke.

Differential modulation of reciprocal inhibition in ankle muscles during rhythmic arm cycling

Interlimb neural linkages relay activity related to rhythmic arm movement to the lumbar spinal cord. This is detected by modulated reflex amplitudes in muscles remote from the rhythmic movement. Improved understanding of modulation in ankle flexor and extensor muscles due to rhythmic arm movement can be gained using modulation of spinal excitability as a probe. The modulatory effect of rhythmic arm movement on Ia reciprocal inhibition (RI) between functional antagonists at the ankle has not been studied. We investigated the influence of rhythmic arm cycling on short latency (∼55ms post-stimulus) RI between ankle flexor (tibialis anterior, TA) and extensor (soleus, SOL) muscles at varying (0.9, 1.0, 1.2, 1.5 and 2.0× motor threshold (MT)) stimulus intensities. We hypothesized that arm cycling would increase RI between antagonists, but that movement conditioning would vary depending on stimulus intensity used to evoke the RI response. Amplitude of RI deduced from suppression of ongoing EMG activity was compared in static and arm cycling conditions. Arm cycling significantly (p<0.05) increased RI in SOL at 1.0×MT, but had no effect in TA at any stimulus intensity (p>0.05). Descending signals arising from rhythmic arm movement significantly alter transmission in RI pathways between ankle flexor and extensor muscles differentially. This may be due to differences in descending supraspinal inputs to ankle flexors vs. extensors, and could be related to functional requirements during locomotion.

Modulation of reciprocal inhibition between ankle extensors and flexors during walking in man.

1. The modulation of disynaptic reciprocal inhibition between antagonistic ankle muscles during walking was investigated in 17 healthy human subjects. Inhibition from ankle dorsiflexors to ankle plantar flexors was evoked by stimulation of the common peroneal nerve (CPN) and evaluated as the stimulus-induced depression of rectified soleus EMG activity (latency approx. 40 ms) or the short-latency depression of the soleus H-reflex (conditioning-test intervals around 2-3 ms). In some experiments the inhibition from ankle plantar flexors to ankle dorsiflexors was investigated. In these experiments the tibial nerve was stimulated and the amount of inhibition was evaluated from the short-latency depression of the voluntary rectified tibialis anterior (TA) EMG. 2. The short-latency inhibition of the soleus H-reflex following the CPN stimulation (1.1 x motor threshold; MT) was strongly modulated during walking, being large in the swing phase and absent in the stance phase. 3. A smaller amount of EMG depression following the CPN stimulation (1. 1-1.2 x MT) was observed in the stance phase of walking as compared to tonic or dynamic plantar flexion at a similar background EMG activity level in standing or sitting subjects. 4. In four subjects a depression of the TA EMG activity was produced by stimulation of the tibial nerve (1.1-1.2 x MT). In all subjects a smaller amount of inhibition was observed in the swing phase of walking as compared to tonic dorsiflexion at a comparable EMG activity level. 5. It is concluded that the transmission in the disynaptic Ia reciprocal pathway between ankle plantar flexors and dorsiflexors is modulated during walking. Inhibition from dorsiflexors to plantar flexors seems to be large in swing and small in stance, whereas inhibition from plantar flexors to dorsiflexors seems to be small in swing.

Modulation of reciprocal inhibition and the soleus H-reflex during voluntary movement in spastic patients

Modulation of reciprocal inhibition and the soleus H-reflex during voluntary movement in spastic patients